Kinase inhibitor therapy against genomically selected cancer cell lines can result in death of a substantial proportion of cells, but in nearly all cases resistance to targeted cancer therapies is observed. This resistance can be observed with different kinetics and can be due to a variety of cellular mechanisms but ultimately results in treatment failure. This phenomenon is observed both in pre-clinical cellular and animal models and in patients treated with these classes of drugs. Prior work has shown that cancer cell lines dependent on Fibroblast Growth Factor Receptor (FGFR) amplifications, mutations, and fusions readily acquire resistance when treated with selective FGFR inhibitors, such as BGJ398 and AZD4547, and less selective FGFR inhibitors, such as ponatinib and pazopanib (Wang et al., Oncogene, 2015, 34(17):2167-77). There is a need to find new treatments for proliferative diseases that are or may become resistant to kinase inhibitors.